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Year 4 PAEDS > Conditions 2 > Flashcards

Conditions 2 Flashcards

1
Q

What are the characteristics of febrile seizures? (are they harmful?)

A
  • Generalised tonic-clonic seizures, dont last long.
  • Period of postictal drowsiness
  • Periods of cyanosis/apnoea.

Majority are harmless! 30-40% will develop further febrile seizures.

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2
Q

What are atypical febrile seizures?

A

> 15mins, or >2 within 24hrs, or a focal seizure.

^risk of epilepsy

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3
Q

Management of a febrile seizure?

A

TIME it, + prevent child from hurting themselves (don’t restrain)

  • > 5mins = Buccal midazolam
  • Another 10mins= IV Lorazepam
  • > 30mins= treat as status epilepticus
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4
Q

What are the 2 types of Breath Holding Attacks in toddlers?

A
  1. Cyanotic spells (breath holding episode)

2. Pallid spells (reflex anoxic seizure)

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5
Q

What is the difference of a breath-holding episode + a reflex anoxic seizure?

A
  • Breath-holding: precipitated by anger/crying > holds breath > goes blue > then limp, rapid recovery (absence of postictal phase)
  • Reflex anoxic: precipitated by pain/minor injury > triggers vagal reflex + stops breathing > goes pale > brief seizure sometimes > rapid recovery (absence of postictal phase)
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6
Q

What are generalised epileptic seizures?

A

Discharge arises from both hemispheres.

  • Tonic-clonic (grand mal)
  • Absence (petit mal)
  • Myoclonic
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7
Q

1) Tonic clonic seizures?
2) Absence seizures?
3) Myoclonic seizures?

A

1) Tonic: LoC, limbs extend, back arches + breathing stops. Teeth clenched. Clonic: Intermittent jerking, irregular reathing + micturition. Postictal depression.
2) Fleeting impairments of consciousness, child assumed daydreaming.
3) Shock-like jerks, can result in sudden falls. Common in children with structural neurological disorder.

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8
Q

What are some types of focal epileptic seizures?

A
  • Simple partial: twitching/jerking one side of face/arm/leg. Consciousness retained. Jacksonian march. Sometimes progresses to full tonic-clonic.
  • Complex partial: altered consciousness a/w strange sensations, hallucinations. Commonly chewing, sucking + swallowing movements. Postictal phase.
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9
Q

What is a Jacksonian march?

A

When jerking starts in one part of the body and spreads.

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10
Q

What are infantile spasms? (West Syndrome!)

A

Form of myoclonic epilepsy but considered separately as have particularly poor prognosis.

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11
Q

Presentation of Infantile spasms?

A
  • Age of onset 3-8months
  • Typical flexion spasms (knife jerk/ ‘salam’ spasms) lasting few secs, in clusters up to 30mins.
  • Usually occur on waking from sleep.
  • ?Hx perinatal complications (meningitis/asphyxia)
  • Following onset= developmental regression.
  • EEG characteristic ‘hyperrhythmic’ (chaotic) pattern.
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12
Q

What genetic association is a/w infantile spasms?

A

SCN1A mutation!!!

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13
Q

EEG is indicated when epilepsy is suspected. What are the characteristic patterns for:

  1. Simple absence (petit mal) seizures
  2. Infantile spasms (West syndrome)
A
  1. Three per second spike + wave discharge, B/L synchronous.

2. Hypsarrhythmia, + chaotic background of slow-wave activity.

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14
Q

Management of Infantile Spasms?

A
  • Vigabatrin (1st line)

- ACTH hormone, or prednisolone.

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15
Q

What is the 1st line management of all generalised seizures in children?

A

Valproate

  • Except in females of child bearing age!!
  • Also, if the epilepsy is established + tonic-clonic seizures ONLY then chose : Lamotrigine!
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16
Q

What is not recommended in all generalised seizures apart from tonic-clonic?

A

Carbamazepine, gabapentin or phenytoin.

these are NOT recommended in absense/ myoclonic/ tonic/atonic seizures

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17
Q

What is generally second line in all generalised seizures?

A

Lamotrigine

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18
Q

What is 1st line mx in focal seizures?

A

Lamotrigine!

Also can use: Carbamazepine, Valproate.

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19
Q

What are the key s/e of Valproate?

A
  • Wt gain, hair loss
  • Rare idiosyncratic liver failure (need to monitor LFTs)
  • High teratogenic potential (Pregnancy Prevention Program if no alternative)
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20
Q

What are the s/e of Carbamazepine/Oxcarbazepine?

A
  • Rash, neutropenia, hyponatraemia, ataxia.

- P450 INDUCER!

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21
Q

S/e of Topiramate?

A

Nasty!

-Drowsiness, withdrawal, wt loss.

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22
Q

S/e of Vigabatrin?

A
  • Restriction of visual fields

- Sedation

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23
Q

Mx of Acute Seizures in children?

A
  1. Recovery position. Rectal Diazepam, or Buccal midazolam
  2. If seizure continues >25mins : phenytoin
  3. If seizure continues >45mins : anaesthesia
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24
Q

Tension headaches:

a) Character
b) Timing
c) Mx

A

a) Constricting, band like. Usually develop towards later childhood.
b) End of day. Stress as home/school.
c) Reassurance, paracetamol. Minimise attention to them!

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25
Q

Migraine without aura (90% of migraines):

a) Character
b) Timing
c) Associated features

A

a) Throbbing/pulsatile over temporal/frontal areas. Usually develop late childhood/early teens.
b) Episodic (1-72hrs)
c) GI disturbances, photo/phonophobia. Aggrivated by physical activity!

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26
Q

Management of migraine without aura?

A
  • Rest, simple anaesthesia.
  • Diet control
  • If frequent: prophylactic propranolol/pizotifen.
  • In teens: sumatriptan.
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27
Q

What is the character of a migraine with aura?

A

Headache is preceded by an aura (visual/sensory/motor).
Aura:
-Negative phenomena: hemianopia, scotoma (small areas visual loss)
-Positive phenomena: fortification spectra (zig-zag line)

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28
Q

Mx of migraine with aura?

A

Sleep often relieves.

There is a presence of premonitory sx: tiredness, poor conc., autonomic feats

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29
Q

Red Flags in a child with headache

A
  • Acute onset/ severe pain
  • Fever
  • Intensifies lying down
  • A/w vomiting
  • Regression of developmental skills
  • Consistently U/L pain
  • Cranial bruit
  • HTN or papilloedema
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30
Q

What are some characteristic features of ^ICP or space occupying lesions?

A
  • Worse lying, morning vomiting (without nausea)
  • Night time waking
  • Change in mood/ personality/ educational performance.
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31
Q

Head injury in a child: what advice can be given in a pre-hospital setting?

A

Advise that child must go to hospital if:

  • Any LoC/ seizure
  • High energy head injury
  • Any focal neurological deficit since the injury
  • Any amnesia
  • Any vomiting
  • Safeguarding concerns
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32
Q

What are the signs for a basal skull fracture?

A
  • Panda eyes (peri-orbital bruising)
  • Battle’s sign (mastoid bruising)
  • CSF leaking from nose/ear
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33
Q

What is the difference between non-communicating + communicating hydrocephalus?

A

Non-communicating (obstructive)= obstruction within the ventricular system/ aquaduct.
Communicating= obstruction at the arachnoid villi (site of CSF absorption)

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34
Q

Causes of non-communicating hydrocephalus?

A
  • Congenital: aquaduct stenosis, Dandy-Walker malformation (outflow atresia), Chiari malformation.
  • Posterior fossa neoplasm
  • Intraventricular haemorrhage (in prem)
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35
Q

Causes of communicating hydrocephalus? (failure to reabsorb CSF)

A
  • Subarachnoid haemorrhage

- Meningitis (pneumococcal, TB)

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36
Q

What is hydrocephalus commonly a/w?

A

Neural tube anomalies (occurs in 80% spina bifida)

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37
Q

Presentation of hydrocephalus in infants?

obviously this varies with age + rate in ^ICP

A

Common: irritability, lethargy, poor appetite, vomiting.

  • Accelerated head growth (anterior fontanelle open + bulging, sutures separated)
  • Broad forehead, eyes deviated down (‘setting sun’ sign)
  • Spasticity, clonus + brisk deep tendon reflexes
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38
Q

Management of hydrocephalus?

A
  • Cranial US/MRI/CT
  • Head circumference monitored on centile charts.
  • Intracranial shunts (ventriculoperitoneal)
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39
Q

Difference between Plagiocephaly and Craniosynostosis?

A

Plagiocephaly: asymmetric flattening of one side of skull from positional moulding.
Craniosynostosis: premature fusion of one of more sutures, leading to distortion of head shape.

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40
Q

What is Sturge-Weber Syndrome associated with?

A

-Haemangiomatous facial lesion (port-wine stain), in the distribution of the trigeminal nerve (a/w similar lesion intracranially). Always involves the ophthmalmic division.

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41
Q

Presentation of Sturge-Weber syndrome?

A

Most severe: epilepsy, learning disabilities + hemiplegia.
Less severe: deterioration unusual after 5yrs, may still be seizures/learning difficulties.

-^risk glaucoma

42
Q

What medication can be used for Gilles de la Tourette’s syndrome? (chronic tic disorder)

A

-Clonidine or resperidone.

43
Q

What is Duchenne muscular dystrophy?

A
  • Progressive disorder resulting in death in early 20s.
  • X-linked recessive, Dystrophic gene defect..
  • It is the commonest hereditary neuromuscular disease.
44
Q

Presentation of Muscular Dystrophy?

A
  • Baby boy normal at birth, delayed walking.
  • 4-6yrs: frequent falls, lordotic waddling gait.
  • Enlarged, weak calves.
  • GOWER’s SIGN (characteristic)
  • Creatine kinase level elevated x10
45
Q

What may a rigid flat foot indicate in older children?

A

A RIGID flat foot is pathological:

  • Tendo-Achilles contracture (ankle)
  • Tarsal coalition (lack of segmentation between 1/more bones of foot)
  • Juvenile idiopathic arthritis
46
Q

How does Septic Arthritis present in children? (most common <2yrs)

A
  • Joint usually hot, swollen + acutely tender
  • +/- fever
  • Limited + painful movement of affected joint
  • Joint effusion in peripheral joints
  • Initial presentation may be a limp
47
Q

Mx of septic arthritis?

A
  • IV flucloxacillin

- Joint should be splinted in acute stage, then mobilised to prevent permanent deformity

48
Q

What is ‘transient synovitis’? (a common DDx of septic arthritis)

A

Transient synovitis= ‘irritable hip’, the commonest cause of acute hip pain in children.
2-12yrs, following/accompanying a viral infection.
In a few, TS precedes the development of Perthes disease.

49
Q

What does Reactive Arthritis (commonest form of arthritis in children) usually follow?

A

Extra-articular infections:

  • Children: enteric bacteria (shigella, salmonella, campylobacter)
  • Adolescents: viral (chlamydia, gonococcus), mycoplasma + borrelia burgdorferi (Lyme disease).
  • Rheum. fever + post-strep in developing countries.
50
Q

What is the presentation of reactive arthritis/irritable hip?

A
  • Low grade fever
  • Transient joint swelling (<6wks), usually ankles/knees
  • Acute-phase reactants normal/mildly^, XRays normal
  • Generally transient + good outcome (NSAIDs only)
51
Q

How does Juvenile Idiopathic Arthritis present?

A
  • Gelling (stiffness after rest)
  • Morning joint stiffness + pain
  • Initially min. joint swelling, then subsequent swelling + inflammation.
  • Chronic: proliferation of synovium + swelling of periarticular soft tissues.
52
Q

What are the long term features of Juvenile Idiopathic Arthritis?

A

Bone expansion from overgrowth.
Knee: leg lengthening + valgus deformity.
Hands: digit length discrepancy.

53
Q

(types of JIA)

Characteristics of systemic JIA (Still’s disease)?

A
  • Rarest form
  • Articular: large + small joints affected
  • Extra-articular: remitting fever, macular rash, hepatosplenomegaly, lymphadenopathy, wt loss.
  • Lab results: anaemia, ^neutrophils+platelets.
54
Q

(types of JIA)

Characteristics of Polyarticular JIA?

A
  • Articular: large+small joints affected symmetrically, morning stiffness.
  • Extra-articular: chronic anterior uveitis (5%)
55
Q

(types of JIA)

Characteristics of Pauciarticular/Oligoarticular JIA?

A
  • Commonest form of JRA
  • Articular: <5joints, usually large
  • Extra-articular: asymmetrical growth, chronic anterior uveitis (20%! NEED REGULAR OPTHALM!)
56
Q 
What do Rhesus factor/ antinuclear antibodies say in:
a) Systemic
b) Polyarticular
c) Pauci/Oligoarticular
(JRA)
A

a) Negative
b) RhF-ve, ANA+ve
c) RhF-ve, ANA+ve

57
Q

What are systemic corticosteroids (IV methylprednisolone) used to manage?

A

-Severe polyarthritis as induction agent.
-Systemic arthritis (life-saving)
Avoided if poss to minimise risk of growth suppression + osteoporosis.

58
Q

What is the cause of a Limping Child age 3-5yrs?

A

Hip effusion- usually caused by transient synovitis or infection.

MUST differentiate from septic arthritis!! (difficult on USS, usually need XR)

59
Q

What is Perthes disease?

A

Limping, 5-8yrs, M:F 5:1
Idiopathic necrosis of hip (due to interruption in blood supply, followed by revascularisation + reosification over 18-36months).
13% bilateral

60
Q

What are the Xray findings of a child with Perthes disease?

A

Fragmented flattened femoral head, subsequently becomes fragmented + irregular.

61
Q

Mx of Perthes disease?

A
  • If identified early: bed rest + traction.
  • Severe/late: maintain hip in abduction w/plasters or calipers (femoral head covered by acetabulum to act as mould for re-ossifying epiphysis)
62
Q

What is a Slipped Capital Femoral Epiphysis?

A

Idiopathic fracture through proximal femoral growth plate- results in displacement of epiphysis of femoral head postero-inferiorly.
Limping teenager 12-15yrs, often obese, 1/3 B/L.

63
Q

What is Slipped Capital Femoral Epiphysis associated with?

A

Metabolic endocrine abnormalities (hypothyroidism + hypogonadism)

64
Q

Presentation of Slipped Capital Femoral Epiphysis?

A 
Limp w/hip pain may be referred to knee.
Onset acute (post-trauma) or insidious.
Examination: restricted abduction + internal rotation of hip.
65
Q

Recommended isolation for:

a) Measles
b) Mumps
c) Rubella

A

a) Measles: from onset of catarrhal stage to day 5 of rash.
b) Mumps: until swelling subsides
c) Rubella: none except non-immune women in 1st trimester.

66
Q

What is the recommended isolation for Chicken Pox?

A

Until all lesions are crusted over.

67
Q

What is involved in the ‘5 in 1’ vaccine?

A
  • Diptheria
  • Tetanus
  • Pertussis
  • H influenzae type b (Hib)
  • Polio
68
Q

When should MMR vaccine NOT be given?

A
  • Non-HIV related immunodeficiency.
  • Allergy to neomycin/kanamycin.
  • Hx of anaphylaxis to egg should be given under supervision.
69
Q

Much of the damage caused by meningeal infection results from the host response. What are 3 pathophysiologies of this?

A
  1. Release of inflam. mediators + activated leukocytes –> endothelial damage –> cerebral oedema, ^ICP + decreased cerebral bloodflow.
  2. Inflammatory response –> vasculopathy –> cerebral cortical infarction.
  3. Fibrin deposits may block resorption of CSF by arachnoid villi –> hydrocephalus.
70
Q

What are the main organisms causing meningitis in:

a) Neonates - 3months
b) 1month - 6yrs
c) >6yrs

A

a) Group B strep, E. coli, Listeria monocytogenes.
b) Neisseria meningitidis, Strep pneumoniae, Haemophillus influenzae.
c) Neisseria meningitidis, Strep pneumoniae,

71
Q

What is the difference between where the organism effects in Bacterial + Viral meningitis?

A

Bacterial: usually confined to meninges.
Virus: may invade underlying brain, causing meningoencephalitis.

72
Q

What types of virus cause meningitis in infants/children?

A
  • Mumps virus
  • Coxsackie & echo viruses (enterovirus)
  • Herpes simplex
  • Adenovirus
  • Poliomyelitis (developing countries)
73
Q

General presentation of Meningitis in infants/children?

A
  • Papilloedema rare in children
  • Bulging fontanelle late sign in infants.
  • Neck stiffness not always present.
  • Opisthotonus (arching of back)
74
Q

Viral presentation of Meningitis?

A
  • Preceded by pharyngitis/GI upset
  • Then fever, headache + neck stiffness (not reliable sign)
  • Classical head retraction a late feature (contrasting to adults)
75
Q

Bacterial presentation of Meningitis?

A
  • Early feature = reduction in consciousness level
  • High pitched cry
  • Convulsions in infants
  • In meningococcal disease: petechial haemorrhages > purpuric rash.
76
Q

What do you assume if a febrile child presents with Purpura?

A

Assume to be due to meningococcal sepsis, even if child doesn’t appear unduly ill at time.
-Give IV BENZYLPENICILLIN + transfer to hospital.

77
Q

Mx of viral/bacterial meningitis?

A

Viral: usually self-limiting.
Bacterial: IV cefotaxime/ ceftriaxone 10-14days (3rd gen cephalosporins)
-Also dexamethasone beyone neonatal period!

78
Q

What do household contacts of Neisseria meningitidis receive?

A 
Prophylactic Rifampicin (along w/infected child after Abx).
Haemophilus influenzae injection.
79
Q

Contraindications to a Lumbar puncture in suspected meningitis? (to examine CSF- cloudy in bacterial)

A
  • Signs of raised ICP (papilloedema, low HR, high BP)
  • Focal neuro signs
  • Cardiorespiratory instability
  • Coagulopathy
  • Thrombocytopenia
  • Local infection at site of LP
80
Q

Describe the following signs that are associated with neck stiffness:

a) Brudzinski sign
b) Kernig sign

A

a) Brudzinski sign: flexion of neck w/child supine causes flexion of knees + hips.
b) Kernig sign: when child lying supine w/hips + knees flexed, there is back pain on extension of knee.

81
Q

What are the key differences in the CSF between bacterial + viral meningitis?

A

Colour: cloudy in bacterial, clear in viral.
Protein: ^^in bacterial, ^/-in viral.
Glucose: decreased in bacterial, normal/decreased in viral.

82
Q

What is the commonest long-term complication in VIRAL meningitis?

A

Sensorineural hearing impairment.

83
Q

What are some complications of BACTERIAL meningitis?

A
  • Hydrocephalus (communicating or non-communicating, when blocked ventricular outlet by fibrin)
  • Subdural effusion (a/w haemophilus influenzae + pneumococcal meningitis)
  • Hearing loss
  • Local vasculitis (may lead to CNS palsies)
  • Cerebral infaction (may lead to focal seizures + epilepsy)
  • Acute adrenal failure
84
Q

What are some general causes of purpura/easy bruising?

A
  • Thrombocytopenia (^platelet destruction/consumption, impaired platelet production)
  • Platelet count normal: vascular disorders (CT disorders, meningococcal infection, Henoch-Schonlein purpura, SLE.
85
Q

Presentation of Immune Thrombocytopenic Purpura?

A
  • Acute onset (1-2wks after viral infection)
  • Reduced platelet count, Increased megakaryocytes
  • Petechiae + superficial bruising
  • Mucosal bleeding
  • Child appears clinically well
  • Intracranial haemorrhage in 1%
86
Q

Mx of Immune Thrombocytopenic Purpura?

A
  • If mild: none (usually remit spont. 6-8wks)
  • Platelet transfusion if v low count
  • Supportive mx if becomes chronic ITP (20%)
87
Q

What is Autoimmune thrombocytopenic purpura caused by?

A

Maternal IgG antibodies crossing placenta + damaging foetal platelets –> foetus becomes thrombocytopenic.

88
Q

What is the pathophysiology of Disseminated Intravascular Coagulation (DIC)?

A

-Coagulation pathway activation, leading to diffuse fibrin deposition in the microvasculature + consumption of coagulation factors + platelets.

89
Q

What is the commonest cause of activation of coagulation in DIC?

A

Severe sepsis + shock due to circulatory collapse (e.g. meningococcal septicaemia)

90
Q

What investigation results should point to DIC?

A

When the following coexist:

  • Thrombocytopenia
  • Prolonged PTT/ATPP
  • Low fibrinogen, raised fibrinogen degradation product
  • Raised D-dimer
  • Microangiopathic haemolytic anaemia
91
Q

What is Purpura fulminans associated with?

A
  • Mostly: Meningococcal disease (vasculitis- leads to loss of large areas of skin by necrosis).
  • Also rarely occurs after VZV infection.
92
Q

What is the commonest cause of septicaemia in neonates?

A

Group B strep, or Gram -ve organisms (from birth canal)

93
Q

What is the physiology of septicaemia?

A

Host releases inflammatory cytokines + activates endothelial cells.
(commonest cause in childhood is meningococcal infection, which may/not be accompanied by meningitis)

94
Q

What is the dermatological presentation of chick pox? (varicella)

A

Rash first appears on trunk/face –> progresses to peripheries.
Papules to Vesicles to Pustules + then crusts over.

95
Q

What is the mx for adolescents/adules with a primary infection of chicken pox?

A

Oral valaciclovir

96
Q

What is Parvovirus B19 (‘slapped-cheek syndrome’)?

A

Causes erythema infectiousum or Fifth disease.
Erythema infectiousum:
Viraemic phase (fever, malaise, headache), then characteristic facial rash, then macpap ‘lace’ like rash on trunk/limbs.

97
Q

What is the most serious consequence of Parvovirus?

A

Aplastic crisis- occurs in children with chronic haemolytic anaemias (sick cell/ thalassaemia), and immunodeficiency (malignancy).

98
Q

What is the characteristic presentation of Conjunctivitis from:

a) Gonococcal infection
b) Chlamydia infection?

A

a) First 48hrs of life: purulent discharge w/conjunctival infection + swollen eyelids. Need to culture + IV cephalosporin.
b) 1-2wks of life: purulent discharge + swollen eyelids. PO erythromycin 2wks.

99
Q

Food allergies can be IgE-mediated and non-IgE mediated, what is the difference?

A

IgE-mediated: hx of allergic sx from urticaria to anaphylaxis (10mins after ingestion).
Non-IgE mediated: involves GI tract (D+V, abdo pain, failure to thrive), colic/eczema may be present (usually hours after ingestion).

100
Q

Diagnosis of food allergies?

A

IgE- mediated: skin-prick tests + measure specific IgE Abs in blood (RAST test)
Non-IgE mediated: clinical Hx.
Gold standard (for both): exclusion of relevant food under a dietician’s supervision.

Year 4 PAEDS (5 decks)

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